A major feature of the architecture of the cell surface is the complex carbohydrate structures that are a part of glycoproteins and glycolipids. These complex carbohydrates, as well as the glycosyltransferases that assemble them, have been the object of detailed study, yet their biological role remains uncertain. It has been suggested that these complex carbohydrate structures are one of the major means by which cells communicate with each other. In these models of cell-cell communication, cell surface receptors recognize and bind specific carbohydrate moieties on neighboring cells and through this linkage direct the information flow between cells. The specific cell surface receptors are central to this model of cell-cell communication. Therefore, the finding that glycosyltransferases are located on the cell surface, as well as at the point of complex carbohydrate synthesis in the golgi complex, strongly implicated them as the specific receptors. These models of cell-cell communication are supported by an expanding body of literature which demonstrates that specific changes in carbohydrate structure occur through embryonic development. This has led investigators to suggest that the formation and recognition of these carbohydrate structures are required for normal embryonic development. One group of mutations that is consistent with this prediction are the developmental mutants in the mouse referred to as the T/t complex. When two T/t complex mice are mated, the dividing mouse embryos die at specific stages of development. Although the precise nature of these mutations has not been established, cell surface carbohydrates and their receptors have been implicated. A second line of investigation that has implicated these complex carbohydrate structures in cell-cell interaction comes from detailed analysis of the surface antigens of normal and tumor cells. Malignant cells differ in their surface antigens from normal cells. Careful study of these antigens by monoclonal antibodies has shown that these antigenic variations are due to carbohydrate structure differences in the malignant cells.